COX-1 is present in most tissues as a “housekeeping” enzyme, and maintains normal gastric mucosa and influences kidney function. The inhibition of COX-1 is therefore undesirable. COX-2 is induced by inflammation. COX-2 typically is not present at baseline, but increases in response to inflammation. The inhibition of COX-2 is therefore desirable, and can be achieved using classic NSAIDs and/or specific COX-2 inhibitors. COX-2 has 60% homology with COX-1, and both COX-1 and COX-2 convert arachidonic acid to, for example, prostaglandin.